Pseudomonas organisms are ubiquitous and may be found in water, in soil, and on vegetation. Between 5% and 30% of physiologically normal persons carry Pseudomonas in their gastrointestinal tracts. These organisms frequently are found in hospitals, and the dissemination of these organisms may occur by aerosol, as well as by direct physical contact with patients or contaminated environmental sites. Potential environmental sites in which these organisms can be found growing include distilled water, antiseptic solutions, whirlpools, eyedrops, irrigation fluids, dialysis fluids, and, often, equipment used for inhalation therapy or respiratory care. Pseudomonas also can be found growing in swimming pools, hot tubs, water parks, cosmetics, illicit injectable drugs, and the inner soles of sneakers.

B. cepacia has been recognized increasingly as a cause of sporadic nosocomial outbreaks of infection in intensive care units. Those outbreaks have been traced to contaminated automated peritoneal dialysis machines, blood gas analyzers, povidone-iodine solution, and chlorhexidine. It also is a common cause of colonization and endobronchial infection in patients with cystic fibrosis.

S. maltophilia has caused pneumonia, urinary tract infections, endocarditis, meningitis, and peritonitis in hospitalized patients and in patients with cystic fibrosis. B. pseudomallei is the cause of melioidosis, a disease described in Box 171.1. B. mallei is the cause of glanders, a disease described in Box 171.2.

Pseudomonas organisms usually are noninvasive, even after colonization and infection of the skin. Pseudomonads produce a variety of virulence factors, including an endotoxin,
an enterotoxin, and multiple extracellular enzymes. The Pseudomonas endotoxin is weak compared with the endotoxins produced by other gram-negative organisms, and it may produce a diarrheal syndrome. The Pseudomonas enterotoxin has an unclear role in causing diarrhea in humans.

Pseudomonas produces many extracellular products, including caseinase, collagenase, elastase, exotoxin A, fibrinolysin, gelatinase, hemolysin, lecithinase, lipase, and phospholipase C. The elaboration of these proteolytic enzymes may result in localized necrosis of skin or lung and corneal ulceration. These proteases can degrade numerous plasma proteins, including complement and coagulation factors. Destruction of lecithin and solubilization of this material (i.e., surfactant) may play an important role in the atelectasis seen in pulmonary infections caused by Pseudomonas. A leukocidin that in part may be capsular material has been described, and exotoxin S has been identified as still another virulence factor.

Attachment of Pseudomonas to mucosal surfaces is mediated by a battery of adhesins, which are produced in large quantities in these organisms. P. aeruginosa binds preferentially to normal respiratory mucin, in contrast to other Enterobacteriaceae. Competitive binding inhibition assays suggest that asialo GM₁, an apical membrane receptor expressed by regenerating respiratory epithelial cells, is a receptor for P. aeruginosa and that epithelial repair represents a major event for P. aeruginosa adherence. The glycocalyx (extracellular slime layer) is important in allowing P. aeruginosa organisms to adhere to each other and to form microcolonies that impair phagocytosis and antibiotic activity. Elevated serum concentrations of immunoglobulin
G4 (IgG4) antibodies to opsonic determinants may inhibit normal pulmonary clearance of P. aeruginosa by pulmonary macrophages in vivo. The pathogenicity of P. aeruginosa depends on its ability to resist phagocytosis. The persistence of these organisms in the lungs of patients with cystic fibrosis may be related to factors in the sputum that interfere with the bactericidal activity of fresh, normal serum against this organism.